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Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.

Altaany Z, Yang G, Wang R - J. Cell. Mol. Med. (2013)

Bottom Line: H2 S had little effect on eNOS protein expression in ECs.LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.

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Related in: MedlinePlus

H2S stimulated the phosphorylation of endothelial NO synthase (eNOS) in endothelial cells (ECs). (A) The effect of NaHS treatment on eNOS phosphorylation. ECs were starved in Dulbecco's modified eagles medium (DMEM) medium free of serum for 24 hrs and treated with different concentrations of NaHS for 30 min. Western blot analysis was conducted using anti-phospho-eNOS and anti-total eNOS antibody, n = 3–4, *P < 0.05 versus control. (B) Time-dependent effect of NaHS treatment on the phosphorylation of eNOS. ECs were treated with NaHS (100 μM) for different periods (0–60 min.). At the end of each time-point, cells were collected and proteins lysates were analysed by Western blot, n = 3–4, *P < 0.05 versus control. (C) The effect of NaHS treatment on eNOS expression level in ECs. The ECs were treated with NaHS (100 μM) for 12–36 hrs, and then cells were collected and proteins were subjected to Western blot analysis. n = 3–4, *P < 0.05 versus control.
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fig02: H2S stimulated the phosphorylation of endothelial NO synthase (eNOS) in endothelial cells (ECs). (A) The effect of NaHS treatment on eNOS phosphorylation. ECs were starved in Dulbecco's modified eagles medium (DMEM) medium free of serum for 24 hrs and treated with different concentrations of NaHS for 30 min. Western blot analysis was conducted using anti-phospho-eNOS and anti-total eNOS antibody, n = 3–4, *P < 0.05 versus control. (B) Time-dependent effect of NaHS treatment on the phosphorylation of eNOS. ECs were treated with NaHS (100 μM) for different periods (0–60 min.). At the end of each time-point, cells were collected and proteins lysates were analysed by Western blot, n = 3–4, *P < 0.05 versus control. (C) The effect of NaHS treatment on eNOS expression level in ECs. The ECs were treated with NaHS (100 μM) for 12–36 hrs, and then cells were collected and proteins were subjected to Western blot analysis. n = 3–4, *P < 0.05 versus control.

Mentions: NaHS (50 and 100 μM) treatment markedly increased the phosphorylation of eNOS in ECs (Fig. 2A). The stimulatory effect of NaHS on eNOS phosphorylation was time dependent, and the increase in phosphorylated eNOS appeared at 10 min., peaked at 30 min., and gradually declined to baseline over the period of 1-hr NaHS exposure (Fig. 2B). NaHS treatment up to 36 hrs had no significant effect on eNOS expression level (Fig. 2C).


Crosstalk between hydrogen sulfide and nitric oxide in endothelial cells.

Altaany Z, Yang G, Wang R - J. Cell. Mol. Med. (2013)

H2S stimulated the phosphorylation of endothelial NO synthase (eNOS) in endothelial cells (ECs). (A) The effect of NaHS treatment on eNOS phosphorylation. ECs were starved in Dulbecco's modified eagles medium (DMEM) medium free of serum for 24 hrs and treated with different concentrations of NaHS for 30 min. Western blot analysis was conducted using anti-phospho-eNOS and anti-total eNOS antibody, n = 3–4, *P < 0.05 versus control. (B) Time-dependent effect of NaHS treatment on the phosphorylation of eNOS. ECs were treated with NaHS (100 μM) for different periods (0–60 min.). At the end of each time-point, cells were collected and proteins lysates were analysed by Western blot, n = 3–4, *P < 0.05 versus control. (C) The effect of NaHS treatment on eNOS expression level in ECs. The ECs were treated with NaHS (100 μM) for 12–36 hrs, and then cells were collected and proteins were subjected to Western blot analysis. n = 3–4, *P < 0.05 versus control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3822893&req=5

fig02: H2S stimulated the phosphorylation of endothelial NO synthase (eNOS) in endothelial cells (ECs). (A) The effect of NaHS treatment on eNOS phosphorylation. ECs were starved in Dulbecco's modified eagles medium (DMEM) medium free of serum for 24 hrs and treated with different concentrations of NaHS for 30 min. Western blot analysis was conducted using anti-phospho-eNOS and anti-total eNOS antibody, n = 3–4, *P < 0.05 versus control. (B) Time-dependent effect of NaHS treatment on the phosphorylation of eNOS. ECs were treated with NaHS (100 μM) for different periods (0–60 min.). At the end of each time-point, cells were collected and proteins lysates were analysed by Western blot, n = 3–4, *P < 0.05 versus control. (C) The effect of NaHS treatment on eNOS expression level in ECs. The ECs were treated with NaHS (100 μM) for 12–36 hrs, and then cells were collected and proteins were subjected to Western blot analysis. n = 3–4, *P < 0.05 versus control.
Mentions: NaHS (50 and 100 μM) treatment markedly increased the phosphorylation of eNOS in ECs (Fig. 2A). The stimulatory effect of NaHS on eNOS phosphorylation was time dependent, and the increase in phosphorylated eNOS appeared at 10 min., peaked at 30 min., and gradually declined to baseline over the period of 1-hr NaHS exposure (Fig. 2B). NaHS treatment up to 36 hrs had no significant effect on eNOS expression level (Fig. 2C).

Bottom Line: H2 S had little effect on eNOS protein expression in ECs.LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.

Show MeSH
Related in: MedlinePlus